Targeting STAT3 provides a potential therapeutic strategy for obstructive sleep apnea-related fibrotic heart disease mediated by TSP1.

Cardiac fibroblast reduction is well-tolerated and demonstrates beneficial outcomes after heart injury.

Mechanotransduction signaling analysis suggests that mechanical tension can sensitize, desensitize, and reverse cell responses to biochemical agonists, as well as provide mechano-adaptive targets for regionally specific drug responses.

Two niches contribute to the control of Drosophila blood cell homeostasis through their differential regulation of hematopoietic progenitors.

Macrophage production of MT1-MMP upon MI contributes to adverse cardiac remodeling and worsened function by promoting EndMT via TGFB, suggesting MT1-MMP inhibition as a therapeutic option for patients with MI.

Adult mouse fibroblasts maintain an embryonic gene expression signature, inherited from their organ of origin, that is important for organ homeostasis and fibrosis, and may assist in targeting fibrotic diseases in an organ-specific manner.

Comprehensive scRNA-seq analysis of cardiac stromal cells in healthy and injured hearts reveals novel cell types and non-linear cell dynamics, providing new insights into cardiac inflammation, fibrosis and repair.

Cardiac intercellular communication plays a critical role in diabetic myocardial fibrosis and specific targeting of Hrc^hi fibroblasts may be a potential therapeutic target for diabetic cardiomyopathy.

A novel hydrogel-based platform uses a limited number of cells for tissue generation and offers unique advantages for high-throughput cardiac tissue culture.

Activation of Activin A-expressing progenitor cells emerges as a pivotal mechanism in bone fracture healing, shedding light on a potential therapeutic avenue to augment bone repair processes.